Acute respiratory failure - PowerPoint Presentation

Slide1

Acute respiratory failureSlide2
Slide3

Classification of RF

Type 1

Hypoxemic RF **

PaO2 < 60 mmHg with normal or ↓ PaCO2Associated with acute diseases of the lungPulmonary edema (Cardiogenic, noncardiogenic (ARDS), pneumonia, pulmonary hemorrhage, and collapse

Type 2

Hypercapnic RF

PaCO2 > 50 mmHg

Hypoxemia is common

Drug overdose, neuromuscular disease, chest wall deformity, COPD, and Bronchial asthmaSlide4

Distinction between Acute and Chronic RF

Acute RF

Develops over minutes to hours

↓ pH quickly to <7.2 Example; Pneumonia

Chronic RF

Develops over days

↑ in HCO3

↓ pH slightly

Polycythemia, Corpulmonale

Example; COPD Slide5

More definitions

Hypoxemia

= abnormally low PaO2

Hypoxia = tissue oxygenation inadequate to meet metabolic needsHypercarbia = elevated PaCO2Respiratory failure may be acute or chronicSlide6

Pathophysiologic causes of Acute RF

●

Hypoventilation

●

V/P mismatch

●

Shunt

●

Diffusion abnormalitySlide7

O

2

CO

2Slide8

Mechanisms of hypoxemia

Alveolar hypoventilation

V/Q mismatch

ShuntDiffusion limitationOther issues we will not considerLow FIO2Low barometric pressureSlide9

F

I

O

2

Ventilation without perfusion

(

deadspace

ventilation)

Diffusion abnormality

Perfusion without ventilation (shunting)

Hypoventilation

NormalSlide10

Perfusion without ventilation (shunting)

Intra-pulmonary

Small airways occluded (

e.g asthma, chronic bronchitis)Alveoli are filled with fluid ( e.g pulm edema, pneumonia)Alveolar collapse (

e.g

atelectasis)Slide11

Dead space ventilation

DSV increase:

Alveolar-capillary interface destroyed e.g emphysema

Blood flow is reduced e.g CHF, PEOverdistended alveoli e.g positive- pressure ventilationSlide12

F

I

O

2

Ventilation without perfusion

(deadspace ventilation)

Diffusion abnormality

Perfusion without ventilation (shunting)

Hypoventilation

NormalSlide13

Hypercarbia

Hypercarbia is always a reflection of inadequate ventilation

PaCO2 is

directly related to CO2 productionInversely related to alveolar ventilation

PaCO2 = k x VCO2

VASlide14

Hypercarbia

When CO2 production increases, ventilation increases rapidly to maintain normal PaCO2

Alveolar ventilation is only a fraction of total ventilation

VA = VE – VDIncreased deadspace or low V/Q areas may adversely effect CO2 removalNormal response is to increase total ventilation to maintain appropriate alveolar ventilationSlide15

Common

causes

Hypoxemic

RF typI

Pneumonia

,

pulmonary

edema

Pulmonary

embolism,

ARDS

Cyanotic congenital heart disease

Hypercapnic

RF

typ IIChronic bronchitis,emphysemaSevere asthma, drug overdosePoisonings, Myasthenia gravisPolyneuropathy, PoliomyelitisPrimary

ms disorders1ry alveolar hypoventilationObesity hypoventilation synd.Pulmonary edema, ARDSMyxedema, head and cervical cord injurySlide16

Brainstem

Spinal cord

Nerve root

Airway

Nerve

Neuromuscular junction

Respiratory muscle

Lung

Pleura

Chest wall

Sites at which disease may cause ventilatory disturbanceSlide17

Causes

1 – CNS

Depression of the neural

drive to breath

Brain stem tumors or vascular abnormality

Overdose of a narcotic, sedative

Myxedema, chronic metabolic

alkalosis

Acute or chronic hypoventilation

and

hypercapniaSlide18

Causes

2 - Disorders of peripheral

nervous system, Respiratory

ms

, and Chest wall

Inability to maintain a level of minute ventilation appropriate for the rate of CO2 production

Guillian-Barre

syndrome, muscular dystrophy, myasthenia gravis, KS, morbid obesity

Hypoxemia and

hypercapniaSlide19

Causes

3 - Abnormities of the airways

Upper airways

Acute epiglotitisTracheal tumors

Lower airway

COPD, Asthma, cystic fibrosis

Acute and chronic

hypercapniaSlide20

Causes

4 - Abnormities of the alveoli

Diffuse alveolar fillinghypoxemic RFCardiogenic and noncardiogenic

pulmonary edema

Aspiration pneumonia

Pulmonary hemorrhage

Associate with Intrapulmonary shunt and increase work of breathingSlide21

Diagnosis of RF

1 – Clinical (symptoms, signs)

Hypoxemia

Dyspnea, CyanosisConfusion, somnolence, fitsTachycardia, arrhythmia

Tachypnea (good sign)

Use of accessory ms

Nasal flaring

Recession of intercostal ms

Polycythemia

Pulmonary HTN, Corpulmonale, Rt. HF

Hypercapnia

↑Cerebral blood flow, and CSF Pressure

Headache

Asterixis

Papilloedema

Warm extremities, collapsing pulse

Acidosis (respiratory, and metabolic)↓pH, ↑ lactic acidSlide22

Respiratory Failure

Symptoms

CNS:

HeadacheVisual DisturbancesAnxietyConfusionMemory LossWeaknessDecreased Functional PerformanceSlide23

Respiratory Failure

Symptoms

Pulmonary:

CoughChest painsSputum productionStridorDyspneaSlide24

Respiratory Failure

Symptoms

Cardiac:

OrthopneaPeripheral edemaChest painOther:Fever, Abdominal pain, Anemia, BleedingSlide25

Clinical

Respiratory compensation

Sympathetic stimulation

Tissue hypoxiaHaemoglobin desaturationSlide26

Clinical

Respiratory compensation

Tachypnoea RR > 35 Breath /min

Accessory musclesRecesssionNasal flaringSympathetic stimulationTissue hypoxiaHaemoglobin desaturationSlide27

Clinical

Respiratory compensation

Sympathetic stimulation

HRBPSweatingTissue hypoxiaAltered mental stateHR and BP (late)Haemoglobin desaturation

cyanosisSlide28

Clinical

Altered mental state

⇓

PaO2 +⇑PaCO2 ⇨ acidosis

⇨

dilatation of cerebral resistance vesseles

⇨

⇑ICP

Disorientation Headache

coma asterixis

personality changesSlide29

Respiratory Failure

Laboratory Testing

Arterial blood gas

PaO2PaCO2PHChest imagingChest x-rayCT

sacn

Ultrasound

Ventilation–perfusion scanSlide30

Distinction between Noncardiogenic (ARDS) and Cardiogenic pulmonary edema

ARDS

Pulmonary edemaSlide31

PaO

2

(kPa)

Hb saturation (%)

8

90

Pulse oximetry

Sources of error

Poor peripheral perfusion

Excessive motion

Carboxyhaemoglobin

or

methaemoglobinSlide32

Case 1

A 36

yo

man who has had a recent viral illness now is admitted to the ICU with rapidly progressive ascending paralysis (diagnosed as Guillain-Barre Syndrome). He is breathing shallowly at 36/min and complains of shortness of breath. His lungs are clear on exam. CXR shows small lung volumes without infiltrates. With the patient breathing room air, ABG are obtained. pH= 7.18 PaCO2= 68 mm Hg PaO2 =49 mm

Hg

HCO3=14mmol/l

His hypoxemia is due to

alveolar hypoventilation

ACUTE RESP FALURESlide33

Endotracheal intubation and positive pressure ventilationSlide34

Indications for intubation and mechanical ventilation

inability to protect the airway

respiratory acidosis (pH<7.2)

refractory hypoxemiafatigue/increased metabolic demandsimpending respiratory arrestpulmonary toiletSlide35

Case 2

A 65

yo

man has smoked cigarettes for 50 yrs. He has chronic cough with sputum production and chronic dyspnea on exertion (stops once when climbing 1 flight of stairs). He is now admitted with several days of increased cough productive of green sputum and is short of breath even at rest. On exam his breathing is labored (32/min) and his breath sounds are quite distant. The expiratory phase is greatly prolonged and there are soft wheezes in expiration.

chronic respiratory acidosis

pH=7.38

PCO2=48

PO2=48

O2 sat=78%

HC03=38mmol/l

His hypoxemia is

predominantly due to V/Q mismatchSlide36

Case 2- treatment

Supplemental oxygen

Nasal canula

Humidified maskVenturi maskReservoir maskEndotracheal tubeThe goal of therapy is to achieve adequate oxygen content for O2 delivery.Slide37

Case 2 - treatment

The patient received 100% oxygen by reservoir mask and a small dose of medication to help him relax.

One hour later he is hard to arouse and his ABG shows

pH 7.25, PaCO2 64, PaO2 310Has he improved?What is his acid-base status now?What happened?Slide38

Oxygen therapy

Like most other therapies, Oxygen therapy has both benefits and risks

Potential complications of oxygen therapy

Acute lung injuryRetrolental fibroplasiaDecreased respiratory drive in individuals with chronic hypercarbiaUse the lowest possible FIO2 to achieve adequate O2 saturation for oxygen deliverySlide39

Case 3

A 56

yo

man with known coronary artery disease and a prior myocardial infarction has had 1 hr of substernal chest pressure associated with nausea and diaphoresis. When you first see him, he is sitting upright in obvious distress and is cyanotic. He is breathing 36/min with short, shallow breaths. On examination of the chest he has dense inspiratory rales (crackles) half way up his back on both sides. Cardiac exam reveals faint heart sounds with an S3 gallop. Slide40

Case-3 ABG’s

room air

FIO

2

= 1.0

pH

7.28

7.27

PCO

2

32

33

PO

2

43

76

O

2

sat

A-aO2 gradient

72%

66 mmHg95%Mechanism of hypoxemia  shunt CARDIOGEN PULMONARY EDEMSlide41

Respiratory physiology of congestive heart failure

Vascular congestion

– increased capillary blood volume, mild bronchoconstriction, mild decrease in lung compliance; PaO2 normal or even increased

Interstitial edema – decreased compliance and lung volumes, worsening dyspnea, V/Q abnormality and widened A-a O2 gradientAlveolar flooding – lung units that are perfused but not ventilated, shunt physiology with profound gas exchange abnormalities, decreased compliance and lung volumesSlide42

Treatment of cardiogenic pulmonary edema

Correct the problem with left ventricular function

Diruetics

NitratesVasodilatorsThrombolytics, etc.Decrease work of breathingVentilatory supportImprove oxygenationSupplemental oxygenMechanical ventilationSlide43

Distinction between Noncardiogenic (ARDS) and Cardiogenic pulmonary edema

ARDS

Tachypnea, dyspnea, crackles Aspiration, sepsis3 to 4 quadrant of alveolar flooding with normal heart size, systolic, diastolic function

Decreased compliance

Severe hypoxemia refractory to O2 therapy

PCWP is normal <18 mm Hg

Cardiogenic edema

Tachypnea, dyspnea, crackles

Lt ventricular dysfunction, valvular disease, IHD

Cardiomegaly, vascular redistribution, pleural effusion, perihilar bat-wing distribution of infiltrate

Hypoxemia improved on high flow O2

PCWP is High >18 mmHgSlide44

Management of ARF

ICU admition

1 -Airway management

Endotracheal intubation: IndicationsSevere HypoxemiaAltered mental status

Importance

precise O2 delivery to the lungs

remove secretion

ensures adequate ventilationSlide45

Management of ARF

2 -Correction of hypoxemia

O2 administration via nasal prongs, face mask, intubation and Mechanical ventilation

Goal: Adequate O2 delivery to tissuesPaO2 = > 60 mmHg Arterial O2 saturation >90%Slide46

Management of ARF

4 –

Mechanical ventilation

IndicationsPersistence hypoxemia despite O2supplyDecreased level of consciousnessHypercapnia with severe acidosis (pH< 7.2)Slide47

Management of ARF

4 - Mechanical ventilation

Increase PaO2

Lower PaCO2Rest respiratory ms (respiratory ms fatigue)Ventilator

Assists or controls the patient breathing

The lowest FIO2 that produces SaO2 >90% and PO2 >60 mmHg should be given to avoid O2 toxicitySlide48

Management of ARF

5 -PEEP (positive End-Expiratory pressure

Used with mechanical ventilation

Increase intrathoracic pressureKeeps the alveoli openDecrease shuntingImprove gas exchange

Hypoxemic RF (type 1)

ARDS

PneumoniasSlide49

Management of ARF

6 - Noninvasive

Ventilatory

support (IPPV)Mild to moderate RFPatient should have

Intact airway,

Alert, normal airway protective reflexes

Nasal or full face mask

Improve oxygenation,

Reduce work of breathing

Increase cardiac output

AECOPD, asthma, CHFSlide50

Management of ARF

7 - Treatment of the underlying causes

After correction of hypoxemia, hemodynamic stability

Antibiotics

Pneumonia

Infection

Bronchodilators

(COPD, BA)

Salbutamol

reduce bronchospasm

airway resistanceSlide51

Management of ARF

7 -

Treatment of the underlying causes

PhysiotherapyChest percussion to loosen secretionSuction of airways Help to drain secretion

Maintain alveolar inflation

Prevent atelectasis, help lung expansionSlide52

Management of ARF

8 - Weaning from mechanical ventilation

Stable underlying respiratory status

Adequate oxygenationIntact respiratory driveStable cardiovascular status

Patient is a wake, has good nutrition, able to cough and breath deeplySlide53

Complications of ARF

Pulmonary

Pulmonary embolism

barotrauma pulmonary fibrosis (ARDS)Nosocomial pneumonia

Cardiovascular

Hypotension, ↓COP

Arrhythmia

MI, pericarditis

GIT

Stress ulcer, ileus, diarrhea, hemorrhage

Infections

Nosocomial infection

Pneumonia, UTI, catheter related sepsis

Renal

ARF (hypoperfusion, nephrotoxic drugs)

Poor prognosis

NutritionalMalnutrition, diarrhea hypoglycemia, electrolyte disturbancesSlide54

Prognosis of ARF

Mortality rate for ARDS

→ 40%

Younger patient <60 has better survival rate75% of patient survive ARDS have impairment of pulmonary function one or more years after recovery Mortality rate for COPD

→10%

Mortality rate increase in the presence of hepatic, cardiovascular, renal, and neurological disease